Trypanosomiasis is a term used to describe a group of allied protozoal diseases, each of which is due to infection with a species of the genus Trypanosoma. They reach great importance in Africa where their presence in enzootic form precludes the keeping of domestic animals throughout the largest part of the continent between 15.degree.N and 20.degree.S latitude. The pathogenic trypanosomes of Africa are considered to be primarily associated with the tsetse flies (glossina) which feed on vertebrate blood. The tsetse is the vector and also is the host in which part of the trypanosome life cycle takes part. Wherever tsetse are present, trypanosomiasis will also be found in some part of the mammalian population. The clinical findings are typically those of a wasting disease with intermittent fever. Anemia, edema, and cachexia are parts of the syndrome.
The important trypanosomes pathogenic to domestic animals are T. congolense, T. vivax, T. simiae, T. suis, T. equiperdum, and T. brucei. The latter trypanosome is morphologically identical to T. gambiense, and T. rhodesiense, responsible for human "sleeping sickness" of Africa. The tsetse fly is the vector in the transmittal of these trypanosomes. The trypanosomes T. evansi and T. vivax are also mechanically transmitted by bloodfeeding insects. One trypanosome found in the Western Hemisphere is T. cruzi, which infects both animals and man and in man causes a very serious condition known as Chagas' disease.
Acute Chagas' disease (T. cruzi) occurs in people of all ages but is especially important in the adolescent. The chronic form may be mild and asymptomatic, although it frequently gives rise to myocarditis and N.S. (nervous system) involvement resulting in morbidity and premature mortality.
A recurring problem in the chemotherapy of trypanosomiasis is the patient or animal which relapses after treatment. If the drug fails to clear the circulating parasitaemia or if the parasites reappear in the bloodstream after an aparasitaemic phase which varies depending on the persistence and level of the drugs used, then there is a distinct possibility that either underdosage of the drug is the causative factor or drug resistance has occurred. If, however, there is a prolonged aparasitaemic phase after chemotherapy before the eventual reappearance of the parasite this, in many instances, has been attributed to reinfection if the animal has remained in the endemic area. The other possibility is the existence of an "occult" phase of the disease, which gives rise to a new cycle of parasitaemia.
This was described in greater detail in the case of T. brucei TREU 667/1 infection in the mouse by Jennings, Whitelaw and Urquhart, Parasitol. 75, 143-153 (1977), who found that infections of mice with this stabilate could be cured permanently if treatment was initiated early in the infection (3-7 days) but that if it were delayed (14-21 days), then nearly all the mice eventually relapsed despite the mice being treated with many times the recommended dose of drugs.